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Lecture 48

BPS 334 Lecture 48: renal CORE study guide
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Department
Biomedical and Pharmaceutical Sciences
Course Code
BPS 334
Professor
Dr.Hume

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Description
Fluid and Electrolyte Disorders: Disorders of Sodium, Water, and Potassium Introduction:  2/3 of body water is intracellular  1/3 of body water is extracellular  ¼ of extracellular water (1/12 of total body water) is in the blood vessels (the arterial, venous and capillary systems) called extracellular intravascular fluid ¾ of remaining extracellular/extravascular water is called extracellular interstitial fluid Osmoles: Particles suspended in liquid. In body water, range from large MW (immunoglobulins to low MW (H+ ions). They are cations (Na+, K+, Ca++), anions (Cl-, HCO3-, proteins) or neutral BUN, glucose) Sodium (Na+): Restricted to the extracellular compartments (extracellular conc: 140 mEq/L) Potassium (K+): Restricted to the intracellular compartment by the enzyme Na+/K+/ATPase (intracellular conc: 4 mEq/L Chloride (Cl-): Extracellular anion Phosphate (PO4--): Intracellular anion Urea: Freely crosses cell membranes. Has equivalent intracellular and extracellular concs. **Na+/K+ ATPase: facilitates Na+ entry into extracellular space and K+ entry into cells Osmolality: -Sum of all solute particles per volume of fluid compartment. Expressed in mOsm/kg H O 2 -Although each of the fluid compartments contain different types of solutes, the osmolality of each compartment is the same -This occurs because compartments are separated from each other by membranes that are freely permeable to water -When the osmolality of one compartment rises (becomes hyperosmolar to an adjacent compartment), water flows from the area of hypoosmolality to the area of hyperosmolarity, equalizing the osmolalities on both sides of the membrane -Equalization of different osmolalities on opposite sides of a membrane is a result of water, not of solutes, crossing the membrane Disorders of Sodium: Extracellular Volume Regulation: Total Body Sodium Content: Principal determinant of the extracellular volume. If sodium is added to the body, it can only enter the extracellular space  An increase in total body sodium (ingestion of salty food)  Increase extracellular osmolality relative to intracellular osmolality (hyperosmolar) Water will shift into the extracellular space  Expanding the volume of the extracellular space  A decrease in total body sodium (with the use of diuretics or with gastrointestinal losses as in vomiting or diarrhea)  Decrease the extracellular osmolality (hypoosmolar)  water will shift intracellularly  decreasing the extracellular volume Kidney: Primary regulator of extracellular volume Extracellular Volume Depletion: 1. Extracellular volume decreases 2. Renal perfusion decreases 3. Juxtaglomerular apparatus in the kidney releases renin 4. Renin converts angiotensinogen produced by the liver to angiotensin I; angiotensin I is converted to angiotensin II 5. Angiotensin II causes vasoconstriction and increases aldosterone release form the adrenal gland 6. Aldosterone increases distal renal tubular sodium reabsorption 7. Sympathetic tone, increased with extracellular volume depletion, increases proximal tubular sodium reabsorption Extracellular Volume Expansion: 1. Renin, angiotensin, aldosterone and sympathetic tone decreased 2. Therefore, renal sodium reabsorption decreases and renal sodium excretion increases In a normal individual, renal sodium retention occurs as a response to volume depletion. Renal sodium excretion occurs as a response to volume expansion. Disorders of Sodium: Volume Depletion and Volume Expansion Volume Depletion: Loss of sodium from the body  Extracellular volume depletion  Decreases the extracellular osmolality  Water shifts into cells from extracellular spaces **If volume depletion continues without correction, the extracellular volume will decrease to the extent that organ perfusion will be compromised, leading to cell death** Ways in which your body can become sodium depleted: 1. Sodium loss most commonly occurs from the GI tract with excretion of sodium-rich fluids in the settings of diarrhea or vomiting 2. Sodium loss can also occur with renal losses of sodium, in the settings of diuretic use or with osmotic diuresis (in which renal sodium excretion occurs along with excretion of a high osmolar load) 3. Skin losses: sweating, burns In response to volume depletion, the kidney aggressively reabsorbs sodium in the proximal and distal tubules. **Decreased intake of sodium may make this worse but is unlikely to be a primary cause of volume depletion because of the kidney’s ability to retain sodium. For example, renal sodium excretion drops to zero within a few days of fasting** Sodium Depletion Characteristics:  Low Blood Pressure  Orthostatic Hypotension (drop in BP when in an upright position)  Tachycardia (raise in heart rate)  Major visible veins in the neck are flat rather than full  Skin turgor is decreased (skin remains elevated after being pulled up and released)  Mucous membranes of the nose and mouth are dry  Lungs are clear  No peripheral edema  Patients frequently complain of thirst and dizziness especially in an upright position Sodium Depletion Lab Tests:  High renin, High aldosterone, High ADH, High Catecholamines  Urine sodium low, urine specific gravity high, urine osmolality high, serum BUN/creatinine ratio high Volume Expansion:Always results from decreased renal excretion of sodium **If volume expansion is left uncorrected, engorgement of the intravascular space will lead to malignant hypertension, and passage of fluid into tissue spaces and body cavities  edema** When does inadequate renal excretion of sodium occur? 1. Acute or Chronic Kidney Failure (decreased renal glomerular filtration of sodium and water) 2. Congestive Heart Failure, Cirrhosis, Nephrotic Syndrome a. Heart failure is characterized by an increased extracellular volume which, because of decreased left ventricular function, hemodynamically resembles a decreased effective arterial volume b. When the effective arterial volume is decreased, the renal response is identical to that of actual volume depletion: there is enhanced proximal and distal tubular reabsorption intake of sodium which makes volume expansion worse **In the presence of normal renal function and normal cardiac function, increases in dietary sodium DO NOT cause volume expansion because the renin-angiotensin-aldosterone system is down-regulated  less sodium reabsorption, more sodium excretion** Sodium Expansion Characteristics:  HYPERTENSION (always in renal failure) **heart failure: effects of volume excess may be offset by a decreased cardiac output. BP may be normal or even low  Neck vein distension (jugular venous)  Pulmonary Vascular Congestion (rales)  Ascites (extracellular fluid increase in peritoneal cavitiy)  Edema (facial, pulmonary, peripheral) **fluid in the interstitial space** Disorders of Water: Regulation of Osmolar Concentration Disorders of total body sodium  Volume Disorders Disorders of total body water  Osmolar Disorders Osmolality (conc of solutes in body fluid) is normally between 280-290 mOsm/kg H O 2 -Function of the # of particles in a fluid solution -Small molecules (such as sodium) has the same effect on osmolality as a large molecule. Large molecules therefore do not significantly contribute to osmolality In ECF and ICF: Osmolality = [cations]+[anions] + [neutral particles] But since [cations] = [anions] Osmolality = 2 [cations] + [neutral particles] In ECF (Na+ is by far the most prevalent cation) so… ECF Osmolality = 2 [Na+] + [glucose] + [BUN] Sodium: Prime contributor to osmolality in the extracellular space Potassium: Prime contributor to osmolality in the intracellular space Extracellular Space=overwhelming number of osmoles are electrolytes (Na+, Cl-, HCO3-). Neutral molecules urea nitrogen (BUN) and glucose contribute to a minor extent  Hyponatremia (Na+ conc of below 130 mEq/L) causes Hypoosmolality (osmolality below 280 mOsm/L)  Hypernatremia (Na+ conc of above 145 mEq/L) causes Hyperosmolality (osmolality above 290 mOsm/L) **Hyperosmolality may also be caused by high levels of BUN (as occurs in renal failure) and high levels of glucose (as occurs in uncontrolled diabetes mellitus) ** How do abnormalities in the osmolality and sodium concentrations occur? NOTE: Osmolar changes occur with changes in BODY WATER, NOT with changes in total body solute amount  If sodium chloride (in the form of salt crystals) is ingested, the sodium conc and the osmolality in the extracellular space does increase transiently. But because there is an imbalance between extracellular and intracellular osmolalities and the membranes between the compartments are permeable to water, water moves from the intracellular to the extracellular space, equalizing the osmolalities  Net effect of addition of sodium will be expansion of the extracellular space without a marked increase of the osmolality  Net effect of a decrease in the total body sodium content will similarly decrease the extracellular volume, without significantly decreasing the extracellular osmolality or sodium concentration **Hypoosmolality or hyperosmolality, and hyponatremia or hypernatremia, occur because of abnormalities in body water handling. **Hypoosmolality and hyponatremia are a result of a relative excess of body water. **Hypernatremia is a result of a relative deficit of water. **Hypoerosmolality is a result of a relative water deficit when hypernatremia is present. Disorders of Water: Hypoosmolality ** Hypoosmolality occurs when the plasma osmolality is BELOW 280 mOsm/L and the extracellular sodium concentration is LESS THAN 135 mEq/L Hypoosmolality is a result of a relative excess of total body water and it occurs in two ways: 1. Excess ingestion of water (dilute all fluid compartments and decrease [osm] and [Na+] 2. Decreased excretion of water When extracellular sodium concentration falls below 120 mEq/L, some CNS toxicity occurs including confusion, headache and seizures **Very difficult to become hypoosmolar with increased ingestion of water alone because as water is ingested, the extracellular osmolality does decrease transiently. This slight drop in osmolality suppresses pituitary production of the hormone ADH (a vasopressin). An increase in ADH will increase urine osmolality; as ADH secretion decreases, there is less water absorption, the urine osmolality becomes more dilute and more water is excreted.** Increased water intake is normally matched by increased renal water excretion. However, there are 4 ways hypoosmolality can occur 1. Excessive intake of water may exceed the renal ability to dilute the urine and excrete water a. Requires a chronic water intake of over 12 liters’ daily b. Most people who do this have a psychiatric disturbance termed psychogenic polydipsia and is characterized by hypoosmolality and a maximally dilute urine c. Treatment: water restriction and psychiatric intervention when necessary 2
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